Enhanced Connexin-43 and -Sarcomeric Actin Expression in Cultured Heart Myocytes Exposed to Triiodo-l-thyronine
| Autor: | Mordechai Manoach, Tova Zinman, Vladimir Shneyvays, Asher Shainberg, Shay Moshel, Weismann P, Liaman K. Mamedova, Sawa Kostin, Narcis Tribulova |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Histology
Physiology Connexin Biology Immunofluorescence Cell membrane chemistry.chemical_compound Western blot medicine Animals Myocyte Myocytes Cardiac Cells Cultured Actin Dose-Response Relationship Drug medicine.diagnostic_test Gap junction Cell Biology General Medicine Molecular biology Actins Rats Cell biology medicine.anatomical_structure Gene Expression Regulation chemistry Connexin 43 Thyronine Triiodothyronine |
| Zdroj: | Journal of Molecular Histology. 35:463-470 |
| ISSN: | 1567-2379 |
| Popis: | This study examined whether triiodo-L-thyronine (T3) affects the expression of the major intercellular channel protein, connexin-43, and contractile protein alpha-sarcomeric actin. Cultured cardiomyocytes from newborn rats were treated on day three in culture with 10 or 100 nM T3 and examined 48 and 72 h thereafter. Treated and untreated cells were examined by immunofluorescence and electron microscopy. Expression levels of Cx43 and sarcomeric alpha-actin were monitored by Western blot analysis. Immunofluorescence labeling showed cell membrane location of Cx43 in punctuate gap junctions, whereby fluorescence signal area was significantly higher in cultured cardiomyocytes exposed to T3. This correlated with electron microscopical findings showing increased numbers and size of gap junction profiles, as well as with a significant dose-dependent increase of Cx43 expression detected by Western blot. Immunofluorescence of sarcomeric a-actin was enhanced and its expression increased dose- and time-dependently in T3-treated cultured heart myocytes. However, exposure to the higher dosage (100 nM) of T3 caused mild disintegration of sarcomeric a-actin in some myocytes, suggesting an over-dosage. The results indicate that T3 up-regulates Cx43 and accelerates gap junction formation in cultured neonatal cardiomyocytes. They suggest that thyroid status cannot only modulate the mechanical function of cardiomyocytes but also cell-to-cell communication essential for myocardial electrical and metabolic synchronizations. |
| Databáze: | OpenAIRE |
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